Prenatal alcohol exposure is a leading known cause of mental retardation and learning defects in this country. Developmental timing of alcohol exposures is a determinant of the type and severity of brain damage and learning deficits; different types of learning may be differentially susceptible to alcohol-induced acquisition deficits depending upon the developmental period during which alcohol exposure occurs. Neonatal rats will be used to model human third-trimester alcohol exposure in two experiments that will test four hypotheses: 1) Alcohol exposure restricted to postnatal days (PD) 4-6 will significantly impair acquisition of cerebellar-dependent standard delay eye blink classical conditioning in adult rats; comparable exposure during PD 7-9 will not. 2) Alcohol during PD 4-6 will cause significantly greater Purkinje cell loss than comparable exposure during PD 7-9. 3) Exposure during PD 7-9 will significantly impair acquisition of hippocampally-mediated trace eye blink conditioning. 4) PD 7-9 alcohol exposure will cause significant reductions in the total number of hippocampal CA1 neurons. Demonstration of temporal dissociations between types of alcohol-induce dysmorphology and classical conditioning deficits in rats will generate testable hypotheses related to timing of alcohol insult and resulting learning impairments in humans with known histories of gestational alcohol insult.